Overexpression of miR-224-3p alleviates apoptosis from cerebral ischemia reperfusion injury by targeting FIP200

被引:36
作者
Deng, Yiming [1 ,2 ,3 ]
Ma, Gaoting [1 ,2 ,3 ]
Dong, Qihao [4 ]
Sun, Xuan [1 ,2 ,3 ]
Liu, Lian [1 ,2 ,3 ]
Miao, Zhongrong [1 ,2 ,3 ]
Gao, Feng [1 ,2 ,3 ]
机构
[1] Capital Med Univ, Beijing Tiantan Hosp, Dept Intervent Neuroradiol, Beijing, Peoples R China
[2] China Natl Clin Res Ctr Neurol Dis, Beijing, Peoples R China
[3] Beijing Inst Brain Disorders, Ctr Stroke, Beijing, Peoples R China
[4] Cent Hosp Zibo, Dept Neurol, Zibo, Peoples R China
关键词
apoptosis; FIP200; ischemic stroke; miR-224-3p; EXPRESSION; THROMBECTOMY; MICRORNAS; CANCER; STROKE;
D O I
10.1002/jcb.28975
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Aims In previous studies, numerous differential microRNAs (miRNAs) in cerebral ischemic/reperfusion (I/R) injury were identified using the miRNA microarray analysis. However, the relationship between miRNA and cerebral I/R injury remains largely unknown. In this study, we investigated the function and explored the possible mechanism of miR-224-3p in cerebral I/R injury. Methods Oxygen glucose deprivation model in N2a cells were used to perform the cerebral I/R injury in vitro. Trypan blue staining, reactive oxygen species (ROS) production, and caspase-3 were measured to evaluate the function of miR-224-3p. Results Overexpression of miR-224-3p alleviated the apoptosis induced by oxygen glucose deprivation (OGD) and cleaved caspase-3 was significantly reduced. We further provided the possible mechanism that miR-224-3p may protect cells from cerebral I/R injury by targeting FAK family-interacting protein (FIP200). Further rescue experiment proved that overexpression of FIP200 partially blocked the effect of miR-224-3p. Conclusions We evaluated the function and mechanism of miR-224-3p in ischemic brain injury. miR-224-3p may serve as a potential target for new therapeutic intervention.
引用
收藏
页码:17151 / 17158
页数:8
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